Activating mutation in one of the RAS genes (KRAS, NRAS, and HRAS) drive the development of approximately 30% of all human cancers. Cell stress is a prominent feature of cancer tissues. The hijacking of adaptive mechanisms to cellular  stress by mutant RAS allow tumors to grow  under adverse conditions and are also largely responsible for the notorious drug resistance of RAS cancers to chemotherapeutic agents. Our research is focused on uncovering how mutant RAS coerces stress adaptive mechanisms and how this affects cancer progression and therapeutic response.

Grabocka Lab